| Project/Area Number |
26463010
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Surgical dentistry
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| Research Institution | Hiroshima University |
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Principal Investigator |
Nishi Hiromi 広島大学, 病院(歯), 助教 (70403558)
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| Co-Investigator(Kenkyū-buntansha) |
武知 正晃 広島大学, 医歯薬保健学研究院(歯), 准教授 (00304535)
太田 耕司 広島大学, 病院(歯), 助教 (20335681)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 口腔粘膜疾患 / 口腔粘膜炎症性疾患 / 口腔粘膜 |
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| Outline of Final Research Achievements |
To investigate DNA viral recognition mechanism in oral mucosal cells, we examined the effects of double-strand DNA (dsDNA) derived HSV on anti-viral and inflammatory response in immortalized oral keratinocytes (RT7) and gingival fibroblasts (GT1). We found that CXCL10, a chemokine associated with regulation of T cells, was induced by transfected ds DNA. However, naked dsDNA did not affect the CXCL10 expression. Transfected DNA increased the expression of NF-kB in nuclear fraction, and Ikba inhibitor decreased CXCL10 expression in both cell in dose dependent manner. CXCL10 expression were inhibited by RIG-I siRNA in both cells, whereas IFI16 siRNA decreased CXCL10 expression in GT1, but not RT7. Oral keratinocytes and fibroblasts recognized dsDNA via intercellular receptor to produce anti-viral chemokines through NF-kB activation, and RIG-I and IFI16 may have a role in regulating these immune responses.
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